This research is designed to examine the role and interaction between some vasoactive mediators in the regulation of fetal renal function and its adaptation to extrauterine life. Previous studies on the fetal lamb suggest that the maintenance of homeostasis by the kidney is modulated by the interaction of vasoactive mediators released during asphyxia and the possibility of prolonged biological action if the asphyxial stimulus is severe. The effects of acute perinatal asphyxia on these control processes are being investigated and correlated with hormone levels in the fetus. Renal function and regional circulation are being studied in relation to plasma catecholamines, vasopressin and renin-angiotensin during: (a) normal gestation, labor and in the immediate neonatal period (b) intrauterine asphyxia with or without antagonists, and (c) exogenous administration of vasoactive mediators to the fetus and newborn. Current work indicates that hypoxemia causes disturbances in renal function and is a major stimulus to release of catecholamines, renin activity and vasopressin both in the fetus and newborn. The stress of labor and delivery also leads to increased plasma levels of these hormones, but this is only partially explained by hypoxemia.